Anti-Beclin-1: Mouse Beclin-1 Antibody

Growing evidence indicates that Beclin 1 protein might act as a regulator of the selective turnover of proteins involved in the control of cell growth and proliferation; moreover, Beclin 1-regulated autophagy relates closely to several human diseases. For instance, autophagy can be stimulated by myocardial ischemia, and during reperfusion it is accompanied by upregulation of Beclin 1. In addition, autophagy has been documented in several neurodegenerative diseases, and the elevation of Beclin 1 at the site of injury may represent enhanced autophagy as a mechanism to discard injured cells and reduce damage to cells by disposing of injured components. Another study demonstrated that NPC1 gene deficiency results in increased basal autophagy in human fibroblasts through increased expression of Beclin 1. Increased Beclin 1 levels and elevated autophagy are also observed in other sphingolipid storage diseases characterized by disrupted cholesterol and sphingolipid trafficking. The HSV1-encoded neurovirulence protein ICP34.5 binds to Beclin 1 and inhibits its autophagy function,] suggesting that endogenous amounts of Beclin 1 are important in protecting against viral invasion. Additional evidence shows that ceramide can control autophagy, and that it may be involved in the tamoxifen-dependent increase in Beclin 1 levels. It has been reported that reduced levels of Beclin 1 expression and mono-allelic deletion were observed in human breast cancer cell lines and tissues.³